Download Carbohydrates and appetite control

Carbohydrates and appetite control
John Blundell and Joanna Le Noury
Abstract Many studies have shown that consumption of high
carbohydrate foods can give rise to a clear modulation of the
expression of human appetite. The potency and time course of
the effects of various carbohydrates on satiety vary with the
amount consumed and the chemical structure. There is evidence
that this biological effect can modulate the temporal profile of
hunger and the eating pattern of meals and snacks. One important issue is the action of carbohydrate foods on satiation (within
meals) and satiety (after meals). These effects can be contrasted
with the relatively weaker effects of high fat foods. The physiological mechanisms through which carbohydrates exert an action
on appetite include plasma glucose levels, glucoreceptors,
hepatic glucose metabolism and glycogen stores. Experimental
evidence indicates that the encouragement to eat high carbohydrate (low fat) snacks or high carbohydrate breakfasts can
significantly reduce daily fat intake, limit energy intake, prevent
weight gain and even induce weight loss. It is therefore possible
to design high carbohydrate diets that provide good nutrition
with adequate control over appetite and a beneficial effect on
body weight. (Aust J Nutr Diet 2001;58 Suppl 1:S13–S18)
Appetite control and the satiety cascade
The control of human appetite is based on the balance
between excitatory processes, which initiate eating, and
inhibitory processes, which arise from food consumption
(and other metabolic events). The biological drive to eat
can be linked with the satiating power of food. ‘Satiating
power’ or ‘satiating efficiency’ is the term applied to the
capacity of any consumed food to suppress hunger and to
inhibit the onset of a further period of eating (1,2). Food
brings about this effect by way of certain mediating processes that can be roughly classified as sensory, cognitive,
post-ingestive and post-absorptive (see Figure 1). The
operation of these processes is generated by the impact of
food on physiological and biochemical mechanisms.
Collectively these processes have been referred to as
the ‘satiety cascade’ (3). The way in which food is sensed
and processed by the biological system generates signals
(neural and humoural) that are utilised for the control of
appetite. It follows that any self-imposed or externally
applied reduction in the food supply (creating an energy
deficit) will weaken the satiating power of food. One conFigure 1. The ‘satiety cascade’, a conceptualisation for
understanding the impact of foods on appetite
control and energy intake
Mediating processes
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sequence of this will be the failure of food to adequately
suppress hunger (the biological drive). The satiety cascade appears to operate as efficiently in obese people as in
lean individuals. Hence a normal appetite response to a
reduced energy intake is evident in obese subjects.
Technically, satiety can be defined as that inhibition of
hunger and eating that arises as a consequence of food
consumption. It can be distinguished from satiation which
is the process that brings a period of eating to a halt. Consequently, satiation and satiety act conjointly to determine
the pattern of eating behaviour and the accompanying profile of motivation. The conscious sensation of hunger is
one index of motivation and reflects the strength of satiation and satiety. It is worth keeping in mind that hunger is
a biologically useful sensation. It is a nagging, irritating
feeling that prompts thoughts of food and reminds us that
the body needs energy. Moreover, there is good evidence
that in most cases hunger is related positively to food
intake and is a valid marker of the motivation to eat (4).
For example, after tracking diurnal rhythms of hunger and
eating it was noted that:
the correlation using hunger ratings and intake during the
same hour of the day was r = 0.5 (P < 0.02). That is, hunger
ratings at the start of each hour were correlated with reported
intake in the hour following each hunger rating (5).
Other researchers measuring spontaneous feeding in
humans have concluded that ‘subjective hunger represents
an intermediary step in the cause-effect sequence between
gut filling and cessation of meal ingestion’ (6). Therefore,
the monitoring of hunger, together with energy intake,
constitutes an important feature of the action of carbohydrates on appetite in humans.
Mechanisms of action of carbohydrates on
appetite
Human appetite is controlled by a complex matrix of factors within a psychobiological system that represents the
interaction between physiological processes in the body
and brain, and the social and physical environments (7,8).
The nutritional composition of food is one significant
aspect of the physical environment and there is plenty of
evidence that different types of foods exert differing
actions on the mechanisms responsible for the expression
of appetite (9). Indeed, the demonstration that foods varying in nutrient composition exert differing tendencies to
induce body weight gain (10) implies that nutrients are significant factors in the regulation (or dysregulation) of
appetite. However, which nutrients are measured, and
how? There are strong logical reasons why glucose should
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BioPsychology Group, University of Leeds, UK
J. Blundell, BSc, PhD,CPsychol, FBPsS, Director of Research, Chair of
PsychoBiology
J. Le Noury, BSc, Research Student
Correspondence: J. Blundell, School of Psychology, The University of
Leeds, Leeds LS2 9JT, UK. Email: [email protected]
Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1
S13
be one of the most important nutrients to be monitored. As
Carlson has pointed out: ‘…because the brain controls
eating, it seems reasonable that hunger might be triggered
by a decrease in the brain’s primary fuel’ (11).
The idea that the metabolism of glucose in the body is
related to the existence of hunger and eating is represented
in the glucostatic hypothesis formulated by Mayer (12,13).
It was postulated that the short-term articulation of energy
intake with energy needs is under glucostatic control (14).
In turn, this implies that dietary carbohydrates clearly are
involved in the short-term control of energy intake. Similar views are embodied in the energostatic hypothesis (15),
metabolic control of food intake (16), the glycogenostatic
hypothesis (17) and the energetic concept of appetite (18).
Although the most obvious mechanism is that hunger is
directly related to fluctuations in the concentration of
blood glucose, the relationship between energy intake and
glucose could be mediated via arteriovenous glucose differences, the rate of glucose utilisation in the liver, or the
activation of glucoreceptive neurons in the periphery, or
the brain, or change in the glycogen stores. Evidence for
the role of glucose in the initiation of eating comes from
the detection of transient declines in blood glucose being
related to meal initiation (19) and the observation that
increases in energy intake follow injections of 2-deoxy-dglucose which stimulate glucose deprivation at glucoreceptors (20). Conversely, glucose infusions (particularly
into the hepatic portal system) produce an inhibition of the
tendency to eat (21). After the consumption of a carbohydrate food, the glucose produced could be monitored early
by glucose-detecting interoreceptors in the upper gastrointestinal tract linked to visceral afferent fibres in the vagus
nerve (22). In addition, Oomura (23), has described glucose-sensitive neurons (which decrease their activity in
response to applied glucose) and glucoreceptor neurons
(which are activated) in different parts of the brain, which
presumably provide an interface between the presence of
available glucose and activity in aminergic or peptidergic
neural pathways (8).
Apart from these direct links between the detection of
glucose and neural transmission, an indirect mechanism
has been postulated through which carbohydrate in the
diet could be related to neurochemical activity. This
mechanism relates the proportion of carbohydrate to protein in the diet to the ratio of tryptophan to other large
neural amino acids in plasma, which determines the
uptake of tryptophan into the brain (24). In turn, it is postulated that this leads to an activation of serotoninergic
neurons, which are functionally coupled to eating behaviour and food selection. The evidence for all the stages in
this biobehavioural loop is equivocal (25), but the ingestion of pure carbohydrate certainly alters the ratios of
plasma amino acids (26). The mediator of this alteration is
the glucose-induced release of insulin.
It follows that many mechanisms exist to monitor the
activity of glucose released by ingested carbohydrates.
Therefore, it should be possible to demonstrate a relationship between consumed carbohydrates and a modulation
of the expression of appetite. Although sweet carbohydrates induce some positive feedback for eating through
the induction of oral afferent stimulation by sweet receptors, this should be countered by the potent inhibitory
action via post-ingestive and post-absorptive mechanisms.
Carbohydrates and appetite—experimental
evidence
On the basis of studies on rats it was argued some years
ago that ‘if the cumulative inhibitory effects of carbohydrate on feeding are indeed energostatic…then any
substance that can readily be used by the animal to provide energy should produce an appropriate food intake
compensation over a period of several hours after
loading (15). Studies have shown that this is also the case
for humans. A variety of carbohydrates, including
glucose, fructose, sucrose, maltodextrins and polysaccharides, exert measurable effects when given in a preload or
an experimental meal, i.e. they suppress later intake by an
amount roughly equivalent to their energy value, although
the time course of the suppressive action may vary
according to the rate at which the carbohydrates are
metabolised.
The preload paradigm is a sensitive procedure for disclosing the effects of glucose and maltodextrin (glucose
polymer) on appetite when these carbohydrates are delivered in a natural food product. For example, in a study
using the uncoupling design, the actions of sweetness and
energy content of a yoghurt preload were experimentally
separated by using judicious combinations of glucose,
maltodextrins, high intensity sweeteners, and the yoghurt
base (27). After consumption, feelings of hunger were significantly suppressed by the high energy preloads
(glucose and maltodextrins) to a greater extent than after
the lower energy loads. Reduction of energy intake in the
test meal was proportional to the energy difference
(678 kJ) between the preloads. The accuracy of this
adjustment confirms the frequent, though not universal,
finding that human subjects adjust their voluntary intake
in response to covert manipulations of the carbohydrate
content of a food. In a more recent study, a comparison
was made between preloads containing maltodextrin or
sucrose compared with lower energy loads with similar
taste characteristics. At one hour after consumption, both
high energy preloads had suppressed intake compared
with their low energy counterparts.
Taken together, these and other studies demonstrate
that the preload design is a sensitive procedure for assessing the satiating power of carbohydrates. It appears that
accurate adjustment of subsequent energy intake (often
called energy compensation) is evident for glucose and
maltodextrin. Measurement at one hour seems to be
almost perfect for detecting the effects of these carbohydrates on satiety. However, this interval may not be most
appropriate for other carbohydrates.
Because the amount of energy provided by carbohydrates was manipulated covertly these, and similar
studies, provide important evidence for the physiological
regulation of short-term appetite.
Evidence from meal manipulations
A good deal of evidence for an action of carbohydrates on
appetite control is provided by the preload design using
experimentally manipulated food substances. However,
perhaps the most convincing evidence comes from studies
in which manipulations have been made within a natural
eating pattern. A number of these studies have compared
the effects of carbohydrate and fat.
S14 Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1
For example, a group of healthy male subjects consumed a standard breakfast of 1.84 MJ (440 kcal) or the
same breakfast supplemented with either fat or carbohydrate. The standard breakfast consisted of orange juice,
scones, and fruit yoghurt and was chosen to disguise well
the nutrient manipulations. After consuming the various
breakfasts (on separate occasions one week apart) hunger
was assessed using rating scales for a period of four hours.
The effects were particularly noticeable for a period of
one to three hours after eating. The carbohydrate supplement suppressed hunger and desire to eat but increased
fullness, whereas the fat supplement failed to produce
such effects (28,29). The effects of the supplements were
apparent during a ‘post-ingestive window’ during which
time the physiological processing of the carbohydrate was
taking place and generating physiological satiety signals.
In a later study when a test snack was given to subjects
during the post-ingestive window, the carbohydrate supplement significantly suppressed the snack food
intake (29) (see Figure 2).
In a further series of breakfast manipulations subjects
consumed four realistic isoenergetic (2035 kJ) breakfasts
varying in macronutrient content (two fat-rich, two carbohydrate-rich—low fibre and high fibre) in a random order
on separate mornings. Ratings of appetite and measures of
food consumption were continued for the rest of the day.
The results indicated that the low energy-dense, high carbohydrate breakfasts were strongly satiating compared
with the equi-energetic high fat meals. Figure 3 shows the
change in perceived fullness upon the different breakfasts.
Both fat-rich breakfasts were more palatable but less satiating than the carbohydrate-rich meals and were followed
by greater food intake during the morning (30).
A further interesting study has used a meal design to
illustrate the impact of a high carbohydrate meal on appetite control. In this study a comparison was made between
two methods of inducing an acute energy deficit (exercise
and breakfast omission). Subjects consumed a 2085 kJ
(500 kcal) breakfast (70% carbohydrate) or a low energy
breakfast (267 kJ, 64 kcal) in association with a 40minute period of exercise (70% VO2 max) or a rest
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In a study based on the operations of the satiety cascade (see Figure 1) the effects of high carbohydrate foods
on both satiation and satiety were assessed in a group of
obese women with a mean body mass index (BMI) of
42 kg/m2. The experimental design was superimposed on
a natural meal pattern of lunch, dinner and evening
snacks (32). The obligatory consumption of a high or low
energy lunch gave rise to high or low levels of hunger during the afternoon. At the dinner meal subjects were
allowed to eat to a level of ‘comfortable fullness’ from
either a selection of high carbohydrate foods or (on a separate occasion) a range of high fat foods. The data in
Figure 5 shows that high carbohydrate foods restricted
energy intake at the dinner meal to approximately 2502 kJ
(600 kcal) and therefore exerted a pronounced control
over satiation. On the other hand the high fat foods permitted an intake of approximately 542 kJ (1300 kcal) and
therefore had a very weak effect on satiation. Of course
these effects arise primarily from the differing energy densities of high fat and high carbohydrate foods. However,
Figure 5 also shows that the much smaller intake of carbohydrate foods had an equally strong effect on postingestive satiety as did the huge amount of fat. This study
indicates that high carbohydrate foods can exert a potent
control over appetite both during the eating process itself
(satiation) and in the post-prandial period (satiety).
Figure 3. Changes in perceived fullness after equi-energetic
breakfasts until lunch. From Holt et al. (30)(a)
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Figure 2. Temporal profile of hunger ratings over four
hours following consumption of test breakfasts.
Significant suppression of hunger brought about
by the carbohydrate but not by the fat
supplement. Adapted from Cotton et al. (29)
period. The exercise session or the breakfast omission was
designed to produce a similar energy deficit of approximately 1668 kJ (400 kcal). The results showed that the
absence of the high carbohydrate breakfast produced a
rise in hunger, which was preserved for the whole morning period (Figure 4) and gave rise to a larger energy
intake at lunch. Interestingly the energy deficit produced
by exercise did not increase hunger and did not increase
the lunchtime food consumption (31). This study indicates
that a high carbohydrate intake at breakfast can suppress
hunger and control appetite at a mid day lunch meal.
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(a) Reproduced with permission from Holt SHA, Delargy HJ, Lawton
CL, Blundell JE. The effects of high-carbohydrate vs high-fat
breakfasts on feelings of fullness and alertness, and subsequent food
intake. Int J Food Sci Nut 1999;50:13–28. <http://www.tandf.co.uk>
Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1
S15
Carbohydrate and the satiety index
Evidence from nutritional interventions
Almost 20 years ago it was suggested that ‘it could be of
great value to have tables showing the energy-satiety ratio
of all the common foods to indicate their potential for
causing over nutrition’ (33). Subsequently, the term ‘satiating efficacy’ was proposed ‘as an index to compare the
satiating potency of different foods’ (2).
The results from short-term studies show clearly that carbohydrates exert a marked influence over the expression
of appetite. Real life intervention studies have demonstrated that this degree of appetite control has practical
consequences. In one study, people identified as snackers
were encouraged to eat 25% of their daily energy intake
from high carbohydrate or high fat snacks during separate
three-week periods. The subjects incorporated the snack
foods into their normal eating repertoires and maintained
a normal lifestyle. The study was very carefully monitored to ensure compliance to the experimental
requirements and to assess food intake from the snack
foods and from the rest of the eating pattern. Measures of
total energy intake indicated that food consumption was
physiologically valid and quite in keeping with body size
and the level of physical activity. First, generous consumption of these palatable high carbohydrate foods did
not generate abnormally high energy intakes. Indeed daily
energy intake was an average of 362 kJ (87 kcal) less than
with the high fat snacks—a value that could lead to a
weight gain of approximately 3.6 kg over the course of a
year. Second, the high carbohydrate foods significantly
lowered the total daily fat intake down to a level recommended in the national dietary guidelines (37).
Consequently this high carbohydrate intervention which
was achieved easily exerted a notable control over appetite and the pattern of nutrient intake.
A further measure explored by Holt et al. (34) relates
the satiety response following a food, to the satiety
response following a reference food (white bread). Isoenergetic preloads (1000 kJ) of 38 foods were consumed,
following which subjective ratings of motivation to eat
were completed over two hours. Significant differences in
the satiating effects of the foods were seen, indicating different foods differ in their satiating capacities. This novel
approach quantifies the effects of a food on satiety and
was based on the idea of developing a satiety index analogous to the glycaemic index. These studies showed that
high carbohydrate foods had a high satiety index measured by the area under the satiety curve.
A further measure has been termed the ‘satiety quotient’ which permits a measure of the effect of a food on
satiation (within an eating episode) and satiety (the effect
following eating). This allows the determination of the
degree of suppression of hunger which can be brought
about per unit of food energy consumed (35) and permits
the tracking of changes over time. Using data from a variety of foods freely consumed it was demonstrated that
hunger was reduced more per kilojoule of carbohydrate
food consumed than of high fat food—but the strength of
this varied with time. This finding confirms the proposal
that ‘joule for joule’ carbohydrate is more satiating than
fat (36).
Figure 4. Profiles of hunger across a nine-hour period
following the exercise and breakfast
manipulations. From Hubert et al. (31)(a)
In a series of studies carried out in Scotland, subjects
have been required to increase their consumption of high
carbohydrate breakfast cereals by 60 g per day for twelve
weeks (38). This intervention resulted in a 5.4% reduction
in energy from fat and a 5.1% increase in energy from
starch. In a second study, overweight men (BMI 29.4)
were required to increase high carbohydrate breakfast
cereal intake by 90 g per day (approximately three bowls)
and an increase in carbohydrate consumption from 40 to
47% of total energy resulted (39). The positive changes in
carbohydrate intake were accompanied by small weight
losses.
Figure 5. Average energy intakes from the high fat and high
carbohydrate dinner meals and subsequent
energy intake in response to these meals measured
for the remainder of the day and for the next 24
hours. ** P < .001, significantly different from
carbohydrate. From Lawton et al. (32)(a)
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(a) Reprinted from Appetite, vol 31, Hubert P, King NA, Blundell JE.
Uncoupling the effects of energy expenditure and energy intake:
Appetite response to short-term energy deficit induced by meal
omission and physical activity, pp 9–19, 1998 by permission of the
publisher Academic Press London.
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(a) Reproduced with permission from Lawton CL, Burley VJ, Wales
JK, Blundell JE. Dietary fat and appetite control in obese subjects:
weak effects on satiation and satiety. Int J Obes 1993;17:409–16.
S16 Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1
Taken together these studies show that a high intake of
carbohydrate foods can lower fat intake and does not compromise energy balance.
Habitual high carbohydrate intake
The evidence from short-term manipulations and
medium-term interventions suggests that carbohydrate
foods can exert a substantial effect over the pattern of eating via short-term mechanisms influencing appetite
control. If this is the case then the habitual consumption of
a high carbohydrate diet should exert a healthy control
over energy balance. In particular the habitual intake of
high carbohydrate foods should help to prevent the development of a positive energy balance and therefore protect
against weight gain.
The analysis of different patterns of nutrient intake can
be carried out using large scale surveys in national databases. However, in these analyses it is necessary to take
account of the serious problem of misreporting, usually
under-reporting, which is a consequence of the form of
data collection (40). This was achieved in an analysis of
one UK national database (41), by excluding all subjects
whose
reported
intakes
were
physiologically
inappropriate (42). Using the data from subjects whose
food intake records were believable, a comparison was
made of subjects (aged 18 to 54 years) who were habitual
consumers of high carbohydrate foods or high fat foods.
Figure 6 shows that among the high carbohydrate consumers, only one person reached a BMI of 30 which
normally is regarded as a cut-off point for obesity. On the
other hand, among the low carbohydrate, high fat consumers the level of obesity was 19 times higher.
Taken together, the experimental manipulations, nutritional interventions and dietary surveys indicate that
carbohydrate foods markedly influence the expression of
appetite and can control the pattern of eating. These foods
can help to prevent people developing a positive energy
balance and can therefore protect against weight gain.
High carbohydrate foods can therefore function as protection factors, which oppose dietary risk factors and help to
prevent the loss of appetite control. However, it should be
recognised that this link between carbohydrate and appetite control does not constitute a biological inevitability. In
certain cases an individual could over-ride physiological
signals and reach a high energy intake on carbohydrate
foods (or beverages). Many routes to weight gain are
possible (43). However, carbohydrate over-eating is probably an exception and in general carbohydrate foods
provide considerable protection against the possibility of
over-eating, positive energy balance and weight gain.
References
1.
Blundell JE, Rogers PJ, Hill AJ. Evaluating the satiating power of
foods: implications for acceptance and consumption. In: Solms J,
editor. Chemical composition and sensory properties of food and
their influence on nutrition. London: Academic Press, 1987. p.
205–19.
2.
Kissileff HR. Satiating efficiency and a strategy for conducting
food loading experiments. Neurosci Biobehav Rev 1984;8:129–35.
3.
Blundell JE, Hill AJ, Rogers PJ. Hunger and the satiety cascade—
their importance for food acceptance in the late 20th century. In:
Thompson DMH, editor. Food acceptability. Amsterdam: Elsevier;
1988. p. 233–50.
4.
Flint A, Raben A, Blundell JE, Astrup A. Reproducibility, power
and validity of visual analogue scales in assessment of appetite sensations in single test meal studies. Int J Obesity 2000;24:38–48.
5.
Mattes R. Hunger ratings are not a valid proxy measure of reported
food intakes in humans. Appetite 1990;15:103–13.
6.
De Castro JM, Elmore DK. Subjective hunger relationships with
meal patterns in the spontaneous feeding behaviour of humans: evidence for a causal connection. Physiol Behav 1988;43:159–65.
7.
Blundell JE. The biology of appetite. Clin Appl Nutr 1991;1:21–31.
8.
Blundell JE. Pharmacological approaches to appetite suppression.
Trends Pharmacol Sci 1991;12:147–57.
9.
Blundell JE, Rogers PJ, Hill AJ. Uncoupling sweetness and calories: methodological aspects of laboratory studies on appetite
control. Appetite 1988;11:54–61.
10. Tremblay A, Plourde G, Despres J-P, Bouchard C. Impact of dietary
fat contents and fat oxidation on energy intake in humans. Am J
Clin Nutr 1989;49:799–805.
Figure 6. Frequency distribution of body mass index (BMI)
among high carbohydrate, low fat consumers (A)
and low carbohydrate, high fat consumers (B).
Adapted from Macdiarmid et al. (42)
A
Overview
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11. Carlson NR. Physiology of behaviour, 5th ed. Boston: Allyn &
Bacon; 1991. p. 411.
12. Mayer J. Gluostatic mechanism of the regulation of food intake. N
Engl J Med 1953;249:13–6.
B
1RRI6XEMHFWV
13. Mayer J. Regulation of energy intake and body weight. Ann N Y
Acad Sci 1955;63:15–43.
14. Van Itallie TB. The gluostatic theory 1953-1988: roots and
branches. Int J Obes 1990;14 Suppl 3:1–10.
15. Booth DA. Postabsorptively induced suppression of appetite and
the energostatic control of feeding. Physiol Behav 1972;9:199–202.
16. Friedman MI. Metabolic control of calorie intake. In: Friedman MI,
Tordoff MG, Kare MR, editors. Chemical senses. Appetite and
nutrition. Volume 4. New York: Marcel Dekker; 1991. p. 19–38.
%0,NJP
17. Astrup A, Flatt JP. Metabolic determinants of body weight regulation. In: Bouchard C, Bray GA, editors. Regulation of body weight:
Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1
S17
biological and behavioral mechanisms. Chichester: John Wiley;
1996. p. 193–210.
18. Blundell JE, Rogers PJ. Hunger, hedonics, and the control of satiation and satiety. In: Friedman M, Kare M, editors. Chemical senses.
Appetite and nutrition. Volume 4. New York: Marcel Dekker; 1991.
p. 127–48.
19. Campfield LA, Smith FJ. Functional coupling between transient
declines in blood glucose and feeding behaviour: temporal relationships. Brain Res Bull 1986;17:427–33.
20. Thompson DA, Campbell RG. Hunger in humans induced by 2deoxy-D-glucose: glucoprivic control of taste preference and food
intake. Science 1977;198:1065–8.
21. Novin D, Vanderweele DA, Rezek M. Hepatic-portal 2-deoxy-Dglucose infusion casues eating: evidence for peripheral glucoreceptors. Science 1973;181:858–60.
22. Mei N. Intestinal chemosensitivity. Physiol Rev 1985;65:211–37.
23. Oomura Y. Chemical and neuronal control of feeding motivation.
Physiol Behav 1988;44:555–60.
24. Wurtman RJ. Nutrients that modify brain function. Sci Am
1982;243:42–51.
25. Blundell JE, Hill AJ. Nutrition, serotonin and appetite: case study
in the evolution of a scientific idea. Appetite 1987;8:183–94.
31. Hubert P, King NA, Blundell JE. Uncoupling the effects of energy
expenditure and energy intake: Appetite response to short-term
energy deficit induced by meal omission and physical activity.
Appetite 1998;31:9–19.
32. Lawton CL, Burley VJ, Wales JK, Blundell JE. Dietary fat and
appetite control in obese subjects: weak effects on satiation and
satiety. Int J Obes 1993;17:409–16.
33. Heaton KW. Dietary fibre and energy intake. In: Berchtold P,
Cairella A, Jacobelli A, Silano V, editors. Regulators of intestinal
absorption in obesity, diabetes and nutrition. Rome: Societa
Editriee Universo; 1981. p. 283–94.
34. Holt SHA, Brand Miller JC, Perocz P, Farmakalidis E. A satiety
index of common foods. Eur J Clin Nutr 1995;49:675–90.
35. Green SM, Delargy HJ, Joanes D, Blundell JE. A satiety quotient: a
formulation to assess the satiating effect of food. Appetite
1997;29:291–304.
36. Rolls BJ, Kim-Harris S, Fischman MW, Foltin RW, Moran TH,
Stoner SA. Satiety after preloads with different amounts of fat and
carbohydrate: implication for obesity. Am J Clin Nutr
1994;60:476–87.
37. Lawton CL, Delargy HJ, Smith FC, Hamilton V, Blundell JE. A
medium-term intervention study on the impact of high- and low-fat
snacks varying in sweetness and fat content: large shifts in daily fat
intake but good compensation for daily energy intake. Br J Nutr
1998;80:149–61.
26. Teff KL, Young SN, Blundell JE. The effect of protein or carbohydrate breakfasts on subsequent plasma amino acid levels, satiety
and nutrient selection in normal males. Pharmacol Biochem Behav
1989;34:829–37.
38. Kirk TR, Burkill S, Cursiter MC. Dietary fat reduction achieved by
increasing consumption of a starchy food—an intervention study.
Eur J Clin Nutr 1997;51:455–61.
27. Rogers PJ, Blundell JE. Separating the actions of sweetness and
calories: effects of saccharin and carbohydrates on hunger and food
intake in human subjects. Physiol Behav 1989;45:1093–9.
39. Crombie N, Kirk TR. Prevention of weight gain and blood cholesterol reduction after consumption of a high carbohydrate food in
men. Int J Obes 1999;23 Suppl 5:657.
28. Blundell JE, Burley VJ, Cotton JR, Lawton CL. Dietary fat and the
control of energy intake: evaluating the effects of fat on meal size
and postmeal satiety. Am J Clin Nutr 1993;57 Suppl:772S–778S.
29. Cotton JR, Burley VJ, Westrate JA, Blundell JE. Dietary fat and
appetite: similarities and differences in the satiating effect of meals
supplemented with either fat or carbohydrate. J Hum Nutr Dietet
1994;7:11–24.
30. Holt SHA, Delargy HJ, Lawton CL, Blundell JE. The effects of
high-carbohydrate vs high-fat breakfasts on feelings of fullness and
alertness, and subsequent food intake. Int J Food Sci Nut
1999;50:13–28.
40. Blundell JE. What foods do people habitually eat? A dilemma for
nutrition, an enigma for psychology. Am J Clin Nutr 2000:71:3–5.
41. Gregory J, Foster K, Tyler H, Wiseman M. The dietary and nutritional survey of British adults. London: Her Majesty’s Stationery
Office; 1990.
42. Macdiarmid JI, Cade JE, Blundell JE. High and low fat consumers,
their macronutrient intake and body mass index: further analysis of
the national diet and nutrition survey of British adults. Eur J Clin
Nutr 1996;50:505–12.
43. Blundell JE, Cooling J. Routes to obesity: phenotypes, food choices
and activity. Br J Nutr 2000;83 Suppl 1:S33–S38.
S18 Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1